miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor.
- Author:
Hyosun TAK
1
;
Jihye KIM
;
Aravinth Kumar JAYABALAN
;
Heejin LEE
;
Hoin KANG
;
Dong Hyung CHO
;
Takbum OHN
;
Suk Woo NAM
;
Wook KIM
;
Eun Kyung LEE
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- MeSH: 3' Untranslated Regions; Cell Line; Gene Expression Regulation; Humans; Membrane Potential, Mitochondrial; Membrane Proteins/*genetics; MicroRNAs/*metabolism; Mitochondria/*genetics/*metabolism; *Mitochondrial Dynamics; Mitochondrial Proteins/*genetics; *Protein Biosynthesis; RNA, Messenger/genetics/metabolism
- From:Experimental & Molecular Medicine 2014;46(11):e123-
- CountryRepublic of Korea
- Language:English
- Abstract: Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases, its molecular mechanism is not fully elucidated. In this study, we demonstrate the potential role of miR-27 in the regulation of mitochondrial dynamics. Mitochondrial fission factor (MFF) mRNA is a direct target of miR-27, whose ectopic expression decreases MFF expression through binding to its 3'-untranslated region. Expression of miR-27 results in the elongation of mitochondria as well as an increased mitochondrial membrane potential and mitochondrial ATP level. Our results suggest that miR-27 is a novel regulator affecting morphological mitochondrial changes by targeting MFF.
